imunodefisiensi fix
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IMMUNODEFICIENCY
10703038 10704025 10705001 10705002 10705004 10705028 10705100 10705104 10705120
10705122 10705057 10705019 16207715 10705072 10705026 10705064 10705071 1070504110705008 10705046 10705013 10705113 10705045 10705007 10705053 10705068 1070506910705049 10704062 10704109
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IMMUNODEFICIENCY
Immune disorder
Immune system fails to develop normally orthe immune response is blocked in some way.
Results from:
- embryological developments
problem/ lymphoid organs and
tissues
- infection with virus depress immune function
- treatment/exposure to immunosuppressive agents
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IMMUNODEFICIENCY
Deficiency ofinnate immune mechanism
Complement system deficiencies
Primary immunodeficiencyB-cell deficiency
T-cell deficiency
Combined immunodeficiency
Secondary immunodeficiency
Acquired immunodeficiency syndrome(AIDS)
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IMMUNODEFICIENCY
Primary immunodeficiency
These occurin the human, although somewhat
rarely, as a result of a defect in almost any stage of
differentiation in the whole immune system.
Secondary immunodeficiency
Immunodeficiency may arise as a secondary
consequence of malnutrition, lymphoproliferativedisorders, agents such as X-rays and cytotoxicdrugs, and viral infections.
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PRIMARY IMMUNODEFICIENCYB-cell deficiency
IgA deficiency & Common VariableImmunodeficiency (CVID)
Most common primary immunodeficiencies,represent the extreme ends of a spectrum ofimmunoglobulin deficiencies.
Transient hypo--globulinemia
Immunoglobulin deficiency occurs naturally inhuman infants maternal IgG level . seriousproblem in very premature babies recurrentrespiratory infections, is associated with low IgGlevels which often return somewhat abruptly to
normal by 4 years of age.
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PRIMARY IMMUNODEFICIENCY
T-cell deficiency
No T-cells or poor T-cell function:
- vulnerable to opportunistic infections
- impacts negatively on humoral immunity
- dysfunctional T-cells permit the emergence of
allergies, lymphoid malignancies & autoimmune
syndromes.
Due to: inefficient negative selection in the thymus or
the failure to generate appropriate regulatory cells.
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PRIMARY IMMUNODEFICIENCY
Combined Immunodeficiency
Severe combined immunodeficiency disease (SCID)
involving B-, T- and NK cells.
represents the most severe form of primaryimmunodeficiency defects in cellular and humoralimmunity.
+ severe and recurrent opportunistic infections death.
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SECONDARY IMMUNODEFICIENCY
Immune responsiveness can be depressednonspecifically by many factors.
CMI in particular may be impaired in a state ofmalnutrition. Iron deficiency is particularly important
in this respect, as are zinc and seleniumdeficiencies.
Case
In lepromatous leprosy and malarial infection,
constraint on immune responsiveness imposed bydistortion of the normal lymphoid traffic pathwaysdysfunction of macrophage
Imbalance between Thl and Th2 cells: result ofinfection depress the subset most appropriate for
immune protection.
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RECOGNITION OFIMMUNODEFICIENCY
o Defects in immunoglobulinsquantitative.
2g/L lower limit of normal.
o The humoral immune responsescreening the serum for natural antibodies (Aand B isohemagglutinins, bactericidins against E.coli) attempting to induce active immunizationwith diphtheria, tetanus, pertussis and killedpoliomyelitis-but no live vaccines. CD19, 20 and22 markers enumerate B-cells byimmunofluorescence.
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RECOGNITION OFIMMUNODEFICIENCY
o Patients with T-cell deficiency
hypo- or unreactive in skin tests to such
antigens Active skin sensitization withdinitrochlorobenzene.
o Complement, bactericidal and otherfunctions of polymorphsIn vitro tests.Reduction of nitrobluetetrazolium (NBT) / stimulation of superoxideproduction measure of the oxidative enzymesassociated with active phagocytosis.
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ACQUIRED IMMUNODEFICIENCYSYNDROME
AIDS results from infection by the RNA
retroviruses HN-1 and HN-2.
HIVinfects T-helper cells throughbindingof its envelope gp120 to CD4 and eitherCCR5 or CXCR4 chemokine receptorcofactors. It also infectsmacrophages,microglia, T-cell-stimulating dendritic cells.
chemokines: A family of structurally-related cytokines which selectively induce chemotaxis and activation
of leukocytes. They also play important roles in lymphoid organ development, cell compartmentalizationwithin lymphoid tissues, Th1 /Th2. development, angiogenesis and wound healing.
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Target
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Inti
Gp120
Envelop
HIV
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HIVs Structure
gp120
gp41
Envelop nucleus
p17
p24
p7/p9
RT
Integrase
Protease
RNA HIV
Diploid single
strand
Enzymes
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Siklus Hidup HIV dalam Limfosit-T (CD4)
HIV
RNA
DNA
ds DNA
RT
Integrase
Transkripsi
Proviral DNA
Spliced mRNA
mRNA
Genomic RNA
Polyprotein
Protein
Protease
1
2
3 4
5
6
7
Virion Matang
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AIDS
TheRNAis convertedby thereversetranscriptase to DNA incorporated intothe host's genome dormant until the cell
is activated by stimulators such as TNF.
There is usually a long asymptomatic phaseafter the early acute viral infection has
been curtailed by a CD8CTL immuneresponse. Virus to the lymphoid follicles destroys the dendritic cell meshwork.
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Long asymptomatic phase
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AIDS
CD4 T-helpers, destroys cell mediateddefenses life threatening infections throughopportunist organisms such as Pneumocystiscariniiand cytomegalovirus.
Infection suppresor factors released by Tsinhibit an immune response before Thstimulating the formation of Tc/plasma cell inadequate number.
Immune system VS virus extremely highrates of viral destruction and CD4 T-cellreplacement.
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AIDS
CD4 T-cell depletion: as a result of directpathogenicity, syncytium formation,susceptibility to apoptosis and possiblyother mechanisms.
AIDS: diagnosed in an individual withopportunistic infections, by low CD4 butnormal CD8 T-cells in blood, poor delayed-type skintests, positive tests for viralantibodies and p24 antigen, lymph nodebiopsy and isolation of live virus ordemonstration ofHNgenome by the PCR.
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AIDS
Highly active antiretroviral drug therapy(HAART), combining inhibitors of reversetranscriptase and protease, can eliminatedetectable virus early in disease, althoughlatent virus remains.
Vaccines are being targeted to Th1responses but it is a very difficult virus to
control.
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HIV/AIDS
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Apa ituHIV/AIDS??
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Inti
Gp120
Envelop
HIVH : HumanI : ImmunodeficiencyV :Virus
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Struktur HIV
gp120
gp41
Envelop Inti
p17
p24
p7/p9
RT
Integrase
Protease
RNA HIV
Diploid single
strand
Enzim-enzim
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Target
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AIDS ?
Acquired
ImmunoDeficiency
Syndrom
Didapat
KekebalanPenurunan
Kumpulan
Gejala
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Siklus Hidup HIV
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Mekanisme CD4
Mekanisme pembunuhan sel T-CD4+ telahditeliti secara in vitro pada kelompokLentivirus.
Langsung (Direct)
Tidak Langsung (Indirect)
Mekanisme Lain
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Replikasi virus HIV
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Di bagian tubuh mana HIVberada?
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cairan sperma
darah
HIV didapatkan di
cairan vagina
air susu ibu
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Bagaimana Cara
Penularannya?
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HolmesGoldwater, Network
Hubungan Seks Transfusi darah
Hubungan perinatal (ibu ke janin)
Penggunaan jarum suntik yang
pernah dipakai orang lain
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Resiko penularan per paparan
Transfusi ~80 %Ibu ke anak 1:4
Seks anal (reseptif) 1:30 -1:125
Penasun bersama 1:150
Tertusuk jarum 1:313(petugas kesehatan)
Seks vaginal (reseptif) 1:700
1:2000Seks vaginal (insertif) 1:1000 -1:3000
Terpercik ke sel lendir
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HIV/AIDS tidak menular
melalui
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KONTAK SOSIAL
HIVTIDAK MENULAR MELALUI
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Ciri-ciri Orang dengan HIV+
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PERKEMBANGAN DARI HIV MENJADI AIDS:
3 - 6 BULAN
PeriodeJendela
3 - 10 TAHUN 1 - 2 TAHUN
Tertular
HIV + AIDS
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Hanya dua cara untuk tahu bilaorang itu HIV positif
Orang itu memberitahukan kepada kita.
Melihat tes HIV
Jumlah CD4 yang rendah dengan jumlah CD8sel T yang normal.
Ditemukan antibodi viral dan antigen P24.
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Statistika tentang AIDS
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Penderita HIV-AIDS berdasarkan GolonganUmur Di Kota Bandung Tahun 2007
Berdasarkan kelompok usia, maka kalangan remaja antara 20-29 tahun
merupakan jumlah terbanyak yaitu 67.06 %
GOLONGAN UMUR
30 - 39 th
20.13%
40 - 49 th
4.97%
15 - 19 th
4.55%0 - 14 th
2.27%
50 th
1.01%
20 - 29 th
67.06%
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Penderita HIV-AIDS berdasarkan Profesidi Kota Bandung Tahun 2007
PEKERJAAN
TIDAKDIKETAHUI
3.71%
SWASTA
19.80%
BURUH
KASAR
0.25%
LAIN-LAIN
0.67%IRT
5.98%
MAHASISWA
20.22%
PEKERJA SEX
9.01%
PNS
2.11%
SUPIR
0.25%
TIDAK
BEKERJA
16.01%
WIRASWASTA
21.99%
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Penderita HIV-AIDS berdasarkan Faktorresiko di Kota Bandung Tahun 2006
FAKTOR RESIKO
HOMOSEKSUAL
6.32%
HETEROSEKSUAL
23.08%
PERINATAL2.02%
TIDAK DIKETAHUI
1.26%
IDU
67.31%
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Bagaimana CaraPengobatannya?
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Highly Active Antiretroviral DrugTherapy (HAART) menggabungkaninhibitor reverse transkriptase dan
protease
Dapat mengeliminasi virus pada
tahap awal penyakit namun viruslaten bertahan
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Terima Kasih !